Augmentation of centrally induced alpha-adrenergic vasodepression in spontaneously hypertensive rats.

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Abstract
Central alpha-adrenergic mechanisms for cardiovascular regulation were studied by injecting phenylephrine into a recipient rat whose head was isolated from its body by cross perfusion with a donor rat. Blood pressure increases produced in the donor were accompanied by concurrent reduction of blood pressure and sympathetic nerve activity in the recipient rat's body. These effects were abolished when alpha-adrenergic receptors in the perfused head were blocked with phentolamine. By contrast, intracarotid injections of angiotensin increased blood pressure not only in donor but also in recipient rats. The magnitude of phenylephrine-induced vasodepression was significantly greater in spontaneously hypertensive rats (SHR) than in normotensive or DOCA-salt hypertensive ones. Distribution of radioactive microspheres indicated that carotid arterial blood went mainly to the cerebrum, midbrain, and hypothalamus, with almost negligible amounts going to the lower brainstem. Collectively, our results suggest that centrally administered phenylephrine reduces sympathetic vasomotor tone and blood pressure by acting on alpha-adrenergic receptors located in supramedullary brain areas (possibly in the hypothalamus). In SHR, augmented, vasodepressor responsiveness may be due to reduced brain levels of endogenous norepinephrine that could increase the alpha-adrenergic receptors available.